- Ph.D., Medical Sciences, University of New Mexico Health Sciences Center
Our long-term goals are to clarify the molecular mechanisms contributing to the etiology and pathophysiology of immune complex disease in which chronic complement activation has been demonstrated. These processes are being studied using biochemistry, molecular biology and genetics. Our current emphasis is on the interaction of the two isotypes of the fourth component of complement (C4A and C4B) with the complement receptor CD35/CR1 and the immune complex disease systemic lupus erythematosus (SLE). We are investigating structural differences between the two C4 isoforms, which may affect the clearance, and processing of immune complexes that will ultimately impact the balance between self-reacting B-cells and the normal antibody response.
- Lewis, J.D., B.D. Reilly, and R.K. Bright. 2003. Tumor-associated antigens: From discovery to immunity. Intl. Rev. of Immunol. 22:81-112.
- Reilly, B.D. 2006. Structural comparison of human C4A3 and C4B1 after proteolytic activation by C1s. Mol. Immunol. 43:800-811
- Schraml, B., M.A. Baker, and B.D. Reilly. 2006 A complement receptor for opsonized immune complexes on erythrocytes from Oncorhynchus mykiss but not Ictalarus punctatus. Mol. Immunol. 43:1595-1603